The objective is to investigate the lung toxicity and potential systemic toxicity of particulate gallium arsenide (GaAs), a semiconductor in industrial use. The toxicity of GaAs is unknown yet its industrial use is expanding (and thus the number of people exposed) and it contains the element arsenic, a known toxic metal, that is in an interesting oxidation state (-III) rather than the normal states (+III and +V). Exposure is via inhalation of particles of GaAs and has the potential to cause lung toxicity and/or systemic gallium and arsenic toxicity if it dissolves. Specific aims include determining if GaAs given by intratracheal instillation causes fibrosis in vivo, whether the arsenide (As(-III)) moiety is necessary for toxicity, what the important physical factors are such as particle size and crystal structure, ascertain if other group III - group V semiconductors show similar lung effects and test the hypothesis that GaAs lung effects may be mediated through formation of activated oxygen in a redox reaction. The lung toxicity will be determined by examining lung histology and the lung biochemical parameters of DNA, protein, 4-hydroxyproline, collagen synthesis and degradation, and lipid composition (phospholipids, cholesterol and fatty acid profile) after intratracheal administration of GaAs and several analogous compounds (Ga203, As203, Na3As, Zn3As2, GaN, GaP and GaSb). The potential for activated oxygen will be determined by measuring the levels of endogenous anti-oxidants (glutathione, ascorbic acid) and of enzymes whose function is to deactivate such species (catalase, superoxide dismutase, glutathione peroxidase) after exposure to intratracheal GaAs particulates and appropriate analogous compounds. The biochemical parameters will be correlated with tissue, blood and excretia gallium and arsenic levels.